Understanding and treating feline asthma (Proceedings)
Feline asthma arises from a heterogeneous and poorly characterized group of conditions of the bronchi. "Asthma" is technically caused by reversible bronchospasm (sudden constriction of the smooth muscle of the small bronchi), which is triggered by an underlying inflammatory process. Inflammation in the airway may be brief and transient, or may be a chronic ongoing process. Bronchial inflammation occurs in numerous species, and is mediated by neutrophils, monocytes/macrophages, eosinophils, mast cells and lymphocytes, IgE, histamine, PAF, leukotrienes, prostaglandins, interleukins and TNF. Cats with asthma, like people, seem to have hyper-responsiveness of the airway smooth muscle, and a given stimulus or degree of inflammation leads to a greater degree of bronchospasm in asthmatic cats than it does in normal cats. Clinical signs include coughing and dyspnea, caused by inflammation and bronchospasm.
Chronic inflammation and narrowing of the small bronchi can lead to a number of serious changes in the lung. The lesions in the small bronchi primarily affect expiration. Since the negative pressure exerted by the lung parenchyma on the small bronchi during inspiration tends to "stent" the airways open, inhalation can occur normally. When exhalation occurs, however, the small bronchi tend to collapse because they are narrowed and weakened by inflammation. Early closure of small bronchi during exhalation results in air trapping in the lung and an expiratory respiratory distress. Clinically, lung overdistention with air can be recognized by the presence of over-inflated lungs and a flattened diaphragm on thoracic radiographs. As the lungs become overdistended, emphysema (breakdown of alveolar septal walls) can develop at the periphery of the lungs, leading to decreased alveolar surface area for gas exchange. Persistent mucous plugs in narrowed airways may lead to the development of absorbtive atelectasis (manifested as an alveolar pattern) as the lung collapses distal to the obstructive airway. The right middle lung lobe is particularly susceptible to collapse in asthmatic cats.
Do we know why cats have hyper-responsive airways?Acute and/or chronic inflammation of bronchi occurs in numerous species: canine chronic bronchitis, equine 'heaves", feline asthma/bronchitis and human asthma/bronchitis. Interestingly, smooth muscle hyper-reactivity to inflammation does not occur in all species. It is well documented in cats, horses, and humans, but does not appear to occur in dogs. The reasons for this lack of bronchospasm in the smooth muscle of canine airways are not well understood. One theory involves differences in the innervation of the airway smooth muscle between species. In all species, the airways are innervated by parasympathetic cholinergic pathways which mediate bronchoconstriction, and by sympathetic adrenergic pathways which mediate bronchodilation. Most species also have miscellaneous pathways including tachykinin-containing nerves, rapidly and slowly adapting receptors, and unmyelinated C fibers. In addition, cats, horses and people (but not dogs) have a non-adrenergic vagal inhibitory pathway (NANC) which causes bronchodilation, for which vasoactive intestinal peptide (VIP) and nitric oxide appear to be the mediators. NANC appears to be a remnant of a primitive inhibitory nervous system, which is present in both the GI and the respiratory tracts. In humans, absence of GI NANC leads to loss of inhibition and spasm of GI smooth muscle (Hirschsprung's disease). It is possible that a defect in the NANC system in the feline respiratory tract could result in the hyper-reactive airways we see in feline asthma. Since NANC does not appear to exist in the canine respiratory tract, this could explain the absence of a parallel disease in the dog.
Clinical signs of feline asthma
Classical acute feline asthma is often an eosinophilic inflammatory disorder. These cats have marked acute bronchoconstriction and inflammation that may be triggered by specific allergens. They can present with acute and severe dyspnea. In these cases, once the acute phase has passed and bronchospasm resolves, the animal can return to perfectly normal function, and thoracic radiographs taken after resolution of the crisis will be normal. Clinical signs in these cats are primarily caused by bronchospasm, with an additional contribution from the inflammation. Other cats have more chronic inflammation of the bronchi with infiltrates of inflammatory cells (including neutrophils, eosinophils, or macrophages) that surround the bronchi. Accompanying the inflammatory cells, there is hyperemia and edema of the bronchial mucosa, increased numbers of goblet cells, and increased secretion of mucus. In these cats, a chronic cough is often recognized because the inflammation is ongoing. Intermittent reversible exacerbations of disease may occur, but the underlying inflammatory disease seems to persist between each exacerbation. Thus, thoracic radiographs obtained between incidences of respiratory distress may show varying amounts of peribronchial inflammation.
Differential diagnosis of coughing in cats